The genetic abnormality in the beta cell determines the response to an oral glucose load.
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Effects of novel maturity-onset diabetes of the young (MODY)-associated mutations on glucokinase activity and protein stabilityGenome-edited human stem cell-derived beta cells: a powerful tool for drilling down on type 2 diabetes GWAS biologyNew insights from monogenic diabetes for "common" type 2 diabetesPathogenesis of the metabolic syndrome: insights from monogenic disordersMonogenic diabetes and pregnancyUse of HbA1c in the identification of patients with hyperglycaemia caused by a glucokinase mutation: observational case control studiesEvaluation of serum 1,5 anhydroglucitol levels as a clinical test to differentiate subtypes of diabetesClinical heterogeneity in monogenic diabetes caused by mutations in the glucokinase gene (GCK-MODY).Approach to the patient with atypical diabetes.Assessing the phenotypic effects in the general population of rare variants in genes for a dominant Mendelian form of diabetes.A diagnostic approach for defining idiopathic remitting diabetes: a retrospective cohort study.Mild fasting hyperglycemia in children: high rate of glucokinase mutations and some risk of developing type 1 diabetes mellitus.The Genetic Architecture of Diabetes in Pregnancy: Implications for Clinical Practice.A large multi-centre European study validates high-sensitivity C-reactive protein (hsCRP) as a clinical biomarker for the diagnosis of diabetes subtypes.Identification and functional characterisation of novel glucokinase mutations causing maturity-onset diabetes of the young in Slovakia.Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study: common genetic variants in GCK and TCF7L2 are associated with fasting and postchallenge glucose levels in pregnancy and with the new consensus definition of gestational diabetes mellitus fromA common haplotype of the glucokinase gene alters fasting glucose and birth weight: association in six studies and population-genetics analysesThe development and validation of a clinical prediction model to determine the probability of MODY in patients with young-onset diabetes.Clinical features and treatment of maturity onset diabetes of the young (MODY).Genetic and clinical characteristics of maturity-onset diabetes of the young.Antenatal diagnosis of fetal genotype determines if maternal hyperglycemia due to a glucokinase mutation requires treatmentBest practice guidelines for the molecular genetic diagnosis of maturity-onset diabetes of the young.Defining the genetic aetiology of monogenic diabetes can improve treatment.Phenotypic heterogeneity in monogenic diabetes: the clinical and diagnostic utility of a gene panel-based next-generation sequencing approachMonogenic diabetes in children and young adults: Challenges for researcher, clinician and patient.Clinical application of 1,5-anhydroglucitol measurements in patients with hepatocyte nuclear factor-1alpha maturity-onset diabetes of the young.Differential diagnosis of type 1 diabetes: which genetic syndromes need to be considered?Identification of a novel beta-cell glucokinase (GCK) promoter mutation (-71G>C) that modulates GCK gene expression through loss of allele-specific Sp1 binding causing mild fasting hyperglycemia in humansIdentification of candidate children for maturity-onset diabetes of the young type 2 (MODY2) gene testing: a seven-item clinical flowchart (7-iF).Cross-sectional and longitudinal studies suggest pharmacological treatment used in patients with glucokinase mutations does not alter glycaemia.Common genetic determinants of glucose homeostasis in healthy children: the European Youth Heart Study.Monogenic diabetes: a diagnostic algorithm for cliniciansGlucokinase MODY and implications for treatment goals of common forms of diabetes.GCK Mutation in a Child with Maturity Onset Diabetes of the Young, Type 2.GCK gene mutations are a common cause of childhood-onset MODY (maturity-onset diabetes of the young) in Turkey.Chronic Mild Hyperglycemia in GCK-MODY Patients Does Not Increase Carotid Intima-Media Thickness.Two cases of diabetic ketoacidosis in HNF1A-MODY linked to severe dehydration: is it time to change the diagnostic criteria for MODY?Response to oral gliclazide in a pre-pubertal child with hepatic nuclear factor-1 alpha maturity onset diabetes of the young.Clinical utility gene card for: Maturity-onset diabetes of the young.RD Lawrence lecture 2012: assessing aetiology in diabetes: how C-peptide, CRP and fucosylation came to the party!
P2860
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P2860
The genetic abnormality in the beta cell determines the response to an oral glucose load.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年学术文章
@wuu
2002年学术文章
@zh
2002年学术文章
@zh-cn
2002年学术文章
@zh-hans
2002年学术文章
@zh-my
2002年学术文章
@zh-sg
2002年學術文章
@yue
2002年學術文章
@zh-hant
name
The genetic abnormality in the beta cell determines the response to an oral glucose load.
@en
The genetic abnormality in the beta cell determines the response to an oral glucose load.
@nl
type
label
The genetic abnormality in the beta cell determines the response to an oral glucose load.
@en
The genetic abnormality in the beta cell determines the response to an oral glucose load.
@nl
prefLabel
The genetic abnormality in the beta cell determines the response to an oral glucose load.
@en
The genetic abnormality in the beta cell determines the response to an oral glucose load.
@nl
P2093
P50
P1433
P1476
The genetic abnormality in the beta cell determines the response to an oral glucose load.
@en
P2093
A T Hattersley
M Vaxillaire
O Pedersen
P2888
P304
P356
10.1007/S00125-001-0770-9
P577
2002-03-01T00:00:00Z